2015 HAND BOOK OF MECHANICAL VENTILATION

Editors Stephen Brett Tim Gould Peter McNaughton Zudin Puthucheary Vishal Nangalia ABG Arterial blood gas AC Assist-control ventilation ACT Activated clotting time APRV Airway pressure r

science saving life

foundation

Handbook

of Mechanical Ventilation

A User’s Guide

The Intensive Care Foundation

A User’s Guide

Established in 2003 The Intensive Care Foundation

is the research arm of the Intensive Care Society The

Foundation facilitates and supports critical care research

in the UK through the network of collaborating intensive

care units with the aim of improving the quality of care

and outcomes of patients in intensive care.

The Foundation coordinates research that critically

evaluates existing and new treatments used in intensive

care units with a particular focus on important but

unanswered questions in intensive care The targets for

research are set by our Directors of Research, an expert

Scientific Advisory Board and finally a consensus of the

membership of the Intensive Care Society.

The Foundation also sponsors several annual awards

to encourage and help train young doctors to do

research The outcomes from these research projects are

presented at our national “State of the Art” Intensive

Care meeting in December of each year These include

the Gold Medal Award and New Investigators Awards.

| 5

4 | Contents

First published in Great Britain in 2015

by the Intensive Care Society on behalf of

the Intensive Care Foundation

Churchill House,

35 Red Lion Square,

London WC1R 4SG

Copyright © 2015 The Intensive Care Foundation

All rights reserved No part of this publication may be

reproduced, stored in a retrieval system, or transmitted,

in any form or by any means, electronic, mechanical,

photocopying, recording or otherwise, without prior

written permission of the publisher and copyright owner.

Structure and function of the respiratory system 13

Hypoxaemic (type I) respiratory failure 22

Hypercapnic (type II) respiratory failure 24

Contents | 7

6 | Contents

Classification of O2 delivery systems 47

Endotracheal tubes and

ventilator-associated pneumonia (VAP)

ventilation

89

8 | Contents | 9

Preface

Respiratory problems are commonplace in the emergency department and on the general and specialist wards, and the need for advanced respiratory support represents the most common reason for admission to intensive care An understanding of the approach to patients with respiratory failure and of the principles of non-invasive and invasive respiratory support is thus essential for healthcare professionals, whether nurses, physiotherapists, or doctors When one of the authors of this book began his ICU career,

he sought a short ‘primer’ on mechanical ventilation None

handbook is designed to fill that gap, telling you ‘most of what you need to know’– in a simple and readable format

It is not meant to be exhaustive, but to be a text which can be read in a few evenings and which can then be dipped into for sound practical advice

We hope that you will find the handbook helpful, and that you enjoy working with the critically ill, wherever they may be

The authors, editors and ICF would like to thank Maquet for providing the unconditional educational grant without which the production of this book was made possible No payments were made to any authors or editors, and all profits will support critical care and respiratory-related research

Hugh Montgomery FRCP MD FFICM

Professor of Intensive Care Medicine,

University College London, UK;

Consultant Intensivist, Whittington

Hospital, London, UK

Luigi Camporota MD, PhD, FRCP, FFICM

Consultant Intensivist, Guy’s & St

Thomas’ NHS Foundation Trust.

Orhan Orhan MB BS, BSc, MRCP, FHEA

Specialist Registrar in Respiratory and

General Medicine,

Northwest Thames Rotation, London.

Danny J N Wong MBBS, BSc, AKC, MRCP,

FRCA

Specialist Registrar in Anaesthetics

and Intensive Care Medicine,

King’s College Hospital.

Zudin Puthucheary MBBS BMedSci MRCP

EDICM D.UHM PGCME FHEA PhD

Consultant, Division of Respiratory

and Critical Care Medicine, University

Medical Cluster, National University

Health System, Singapore.

Assistant Professor, Department of

Medicine, Yong Loo Lin School of

Medicine, National University of

Singapore, Singapore.

David Antcliffe MB BS BSc MRCP

Intensive Care and Acute Medicine

Registrar, Clinical Research Fellow,

Imperial College London.

Aman da Joy MBBS BSc MRCGP DCH DRCOG

Specialist Registrar in General Practice,

North East London.

Sarah Benton Luks MBBS DRCOG BSc

GPVTS ST2, sarahluks@gmail.com

Megan Smith LLB, MBBS, FRCA

Specialist Registrar in Anaesthesia and Paediatric Critical Care,

Barts and the London NHS Trust, Whitechapel, London.

Tony Joy MBChB MRCS(Eng) DCH FCEM PGCert

Registrar, London’s Air Ambulance and Barts Health NHS Trust.

Julia Bichard BM BCh MA MRCP

Specialist Registrar in Palliative Medicine, North East London Deanery.

Vishal Nangalia BSc MBChB FRCA; MRC

Clinical Research Training Fellow at UCL;

ST7 Anaesthetics, Royal Free Hospital NHS Trust, London

Katarina Zadrazilova MD

Consultant in Anaesthesia and Intensive care The University Hospital Brno, Czech Republic.

Editors

Stephen Brett Tim Gould Peter McNaughton Zudin Puthucheary Vishal Nangalia

ABG Arterial blood gas

AC Assist-control ventilation ACT Activated clotting time APRV Airway pressure release ventilation

APTT Activate partial thromboplastin time ARDS Acute respiratory distress syndrome

ASB Assisted spontaneous breathing

BiPAP Bilevel positive airway pressure

CaO2 Arterial oxygen content

CI Cardiac index CMV Continuous mandatory ventilation

CO Cardiac output

CO2 Carbon dioxide COHb Carboxyhaemoglobin COPD Chronic obstructive pulmonary disease CPAP Continuous positive airway pressure

CXR Chest x-ray

DO2I Oxygen delivery index ECCO2R Extracorporeal carbon dioxide removal ECMO Extracorporeal membrane oxygenation

Symbols and abbreviations

EPAP Expiratory positive airway pressure

ERV Expiratory reserve volume ETT Endotracheal tube FiO2 Fractional concentration of inspired oxygen

FRC Functional residual capacity

GBS Guillan Barre Syndrome HFOV High frequency oscillatory ventilation

HME Heat and moisture exchanger I:E ratio Ratio of time spent in inspiration to that spent in expiration

IC Inspiratory capacity IPAP Inspiratory positive airway pressure

IPPV Intermittent positive pressure ventilation kPa KiloPascal

mPaw Mean airway pressure

MV Minute ventilation NAVA Neurally adjusted ventilator assist

NIV Non-invasive ventilation

O2 Oxygen

O2ER Oxygen extraction ratio

OI Oxygen Index

12 | Symbols and abbreviations | 13

1 Anatomy and physiology

We offer ventilatory support to:

In our efforts, we must compensate for any loss of airway warming and humidifying functions

Structure and function of the respiratory system

As components of the respiratory system, the airways must

WAFT Air (Warm and Filter Tropical [humidified] Air), and

moist upper airway membranes Failure of warming or humidification leads to ciliary failure and endothelial damage which can take weeks to recover

P(A-a) Alveolar-arterial Oxygen

gradient

PA Pulmonary arteries

Pa Arterial pressure

PaCO2 Partial pressure of carbon

dioxide in arterial blood

PACO2 Alveolar partial pressure of

carbon dioxide

Palv Alveolar pressure

PaO2 Partial pressure of oxygen in

arterial blood

PEEP Positive end expiratory

pressure

Pplat Plateau pressure

PS Pressure support ventilation

Pv Venous pressure

Q Flow

Qc Capillary blood flow

Qs Right ventricular output

which bypasses the lungs

SBT Spontaneous breathing trial SIMV Synchronised intermittent mandatory ventilation SvO2 Percentage saturation of mixed venous blood with oxygen

TLC Total lung capacity V:Q Ratio of pulmonary ventilation to perfusion

VA Alveolar ventilation VAP Ventilator-associated pneumonia

VC Vital capacity VCO2 Carbon dioxide production

VD Dead sapce volume

VE Expired minute ventilation

VO2 Oxygen consumption

VT Tidal volume

Anatomy and physiology | 15

14 | Anatomy and physiology

PAO2 = FiO2 (Patm – pH2O) – PACO2/R

PAO2 and PACO2 are alveolar partial pressures of O2 and

CO2 respectively, FiO2 is the fractional concentration of inspired O2, pH2O is the saturated vapour pressure at body temperature (6.3 kPa or 47 mmHg), Patm is atmospheric pressure and R is the ratio of CO2 production to O2

consumption [usually about 0.8]) The arterial partial pressure of CO2 (PaCO2) can be substituted for its alveolar pressure (PACO2) in this equation as it is easier to calculate Thus, as ventilation falls, alveolar CO2 concentration rises, and alveolar oxygen tension has to fall

Dead space

A portion of each breath ventilates a physiological dead space

gas exchange It has two components:

• Anatomical: the volume which never meets the alveolar membrane (mainly being contained in the conducting airways, or an endotracheal tube);

• Alveolar: the part of tidal volume which reaches areas of the lung which are not perfused – so gas exchange cannot happen;

reaching perfused alveoli each minute is alveolar ventilation

VA = RR x (VT – VD)

Gas exchange begins at the level of the smaller respiratory

bronchioles and is maximal at the alveolar-capillary

membrane – the interface between pulmonary arterial blood

and alveolar air

(NB: The blood supply to the bronchioles remains

unoxygenated About one-third returns to the systemic

venous system, but two-thirds returns to the systemic

arterial circulation via the pulmonary veins, contributing to

the ‘physiological shunt’, below)

Ventilation

Minute ventilation is the volume of gas expired from the

lungs each minute

Minute Ventilation (MV) = Tidal Volume (VT)

x Respiratory Rate (RR)

MV can therefore be altered by increasing or decreasing

depth of the breathing (tidal volume) or RR Of interest, not

you little about ventilation In doing brainstem death

want a more detailed explanation, the simplified alveolar

gas equation offers more detail:

Anatomy and physiology | 17

16 | Anatomy and physiology

In fact, V:Q matching varies in different parts of the lung, and is affected by posture When upright, blood (being a fluid under the influence of gravity) is preferentially directed

to the lung bases, where perfusion is thus greatest But here the pleural pressure is higher, due to the dependant weight

of the lungs, and alveolar ventilation poorest V:Q ratio is thus low The reverse is true at the apex This is probably

enough to know But a more detailed description (if you

really want it) is as follows:

In an upright position, arterial (Pa) and venous (Pv) pressures are highest in the lung bases, and pressures in the alveoli (PAlv) the same throughout the lung, allowing the lung to be divided into three zones:

‘PEEP’ – ☞pages 72-73) In this zone, limited blood flow

means that there is alveolar dead space

In the supine position (how many sick patients are

standing?), the zones are redistributed according to the effects of gravity, with most areas of the lung becoming zone 3 and pulmonary blood flow becoming more evenly

PaCO2 = kVCO2/VA

reduced minute ventilation and/or increased anatomical

dead space or an increase in non-perfused lung

Ventilation/perfusion matching

Deoxygenated blood passes from the great veins to the right

ventricle, into the pulmonary arteries (PA), and then to the

pulmonary capillaries The distribution of blood flow (Q) and

ventilation (V) is closely matched (‘V:Q matching’) throughout

the lung, minimizing physiological dead-space, and

would reach the left ventricle (and thus the arterial tree)

just as deficient in oxygen (deoxygenated) as it was when

it arrived from the veins An area like this which is well

perfused but not adequately ventilated is described as a

physiological shunt Alternatively, imagine one lung having

just dead space – acting as a massive ‘snorkle’!

the systemic circulation, meaning that PA pressure is also

can change locally If alveoli are poorly ventilated, alveolar

(‘Hypoxic Pulmonary Vasoconstriction’ or HPV) and local

blood flow falls In this way, the worst ventilated areas are

also the worst perfused, and V:Q matching is sustained

Anatomy and physiology | 19

18 | Anatomy and physiology

Fig 1

RV ERV TV

IRV IC

FRC

VC TLC

ERV: Expiratory reserve volume – the maximum volume that can be forcibly expired at the end of expiration during normal quiet breathing

RV: Residual volume – the volume of gas left in the lung following a maximal forced expiration

Capacities within the lung are sums of the lung volumes:

FRC: Functional residual capacity – the volume of gas in the lung at the end of normal quiet breathing:

FRC = ERV + RV

VC: Vital capacity – the total volume of gas that can be inspired following a maximal expiration:

VC = ERV + TV + IRV TLC: Total lung capacity – the total volume of gas in the lung at the end of a maximal inspiration:

TLC = IC + FRC

IC: Maximum amount of air that can be inhaled after a normal tidal expiration:

IC = TV + IRV

distributed Positive pressure ventilation increases alveolar

pressure, increasing the size of zone 2

Practical Use of V:Q matching

One lung consolidated from a unilateral pneumonia,

and SaO2 very low? Rolling them onto the ‘good’ side

(i.e., ‘good side down’) means that gravity improves the

blood flow to the best lung – improving V/Q matching,

and thus oxygenation Sometimes, the patient is even

rolled onto their chest (‘prone ventilation’) to help: but

never decide this yourself It’s a big deal, risky in

the turning, and can make nursing very tricky A

consultant decision! Inhaled nitric oxide does a similar

thing: relaxing smooth muscle, well ventilated areas

will benefit from greater ventilation, and by crossing

the alveoli, nitric oxide relaxes vascular smooth muscle,

increasing perfusion to these areas too V:Q matching

increases, and so too does oxygenation Inhaled

(nebulised) prostacyclin is sometimes used to do the

same thing

A brief reminder of lung volume terminology

V T: Tidal volume – the volume of gas inspired / expired

per breath

IRV: Inspiratory reserve volume – the maximum volume

of gas that can be inspired on top of normal tidal volume

20 | Anatomy and physiology | 21

2 Respiratory failure

Respiratory failure is a condition in which the respiratory system is unable to maintain adequate gas exchange to satisfy metabolic demands, i.e oxygenation of and/or elimination

Respiratory failure is generally classified as:

1 Acute hypoxaemic, or type I Low O2 with normal/

low CO2 Most commonly poor V:Q matching (areas

of the lung become poorly ventilated but remain perfused) – e.g pneumonia, pulmonary oedema or

ARDS (☞page 176), or pulmonary embolism (which

redistributes blood flow);

2 Ventilatory, or type II Secondary to failure of the

ventilatory pump (e.g CNS depression, respiratory muscle weakness), characterised by hypoventilation with hypercapnia;

3 Post-operative (type III respiratory failure) is largely a

version of type I failure, being secondary to atelectasis and reduction of the functional residual capacity;

4 Type IV respiratory failure, secondary to hypoperfusion

or shock Blood flow to the lung is inadequate for oxygenation or CO2 clearance

NB: Closing Capacity (CC) is the volume at which

airways collapse at the end of expiration FRC needs to

be >CC for the airways not to collapse at the end of an

expiration

Control of breathing

The respiratory centre that regulates ventilation is located

in the medulla Its output coordinates the contraction of

the intercostal muscles and the diaphragm The respiratory

centre receives inputs from the cerebral cortex, hence

breathing is affected by our conscious state – fear, arousal,

excitement etc There is also input from central (medullary)

and peripheral (carotid body, naso-pharynx, larynx and

pH within normal physiological ranges (and sensitive to

changes in all three such parameters)

Hypoxaemia is mainly sensed by peripheral

chemoreceptors located at the bifurcation of the common

carotid artery A PaO2 below 8 kPa drives ventilation

(‘Hypoxic Ventilatory Response’ or HVR) HVR is higher

when PaCO2 is also raised

Hypercarbia is sensed mainly by central chemoreceptors

(via increases in [H+]) and drives ventilation The response

to a rise in CO2 is maximal over the first few hours and

gradually declines over the next 48 hours, and then further

as renal compensation for arterial pH occurs Hypoxic

ventilatory drive can be important in patients with chronic

lung disease who have a persistent hypercarbia

Respiratory failure | 23

22 | Respiratory failure

Cardiac output (Qt) comprises blood flow through the pulmonary capillaries (Qc) and that bypassing the lung (Qs) Thus, Qt=Qc+Qs The oxygen content of the cardiac output will be Qt x CaO 2 , where CaO 2 is arterial oxygen content This is made up of the oxygen content of the shunt blood (Qs x CvO 2 , where CvO 2 is venous oxygen content) and that of the capillary blood (Qc x CcO 2 , where CcO 2 is the pulmonary capillary oxygen content) With a bit of maths (try it!) you can work out that the shunt fraction (Qs/Qt), = (CcO 2 -CaO 2 )/ (CcO 2 -CvO 2 ), or Qs/Qt= (1-SaO 2 )/(1-SvO 2 )

It is difficult in practice to distinguish between true shunt and Va/Q mismatch However, there is a way of finding out! Va/Q maldistribution results in hypoxaemia because the distribution of alveolar oxygen tension is uneven However, when breathing FiO 2 =1, the alveolar O 2 tension becomes uniform Va/Q scatter has negligible effect on alveolar- arterial O 2 gradient at a FiO 2 =1, and therefore is possible to distinguish the two processes

contri-bute to arterial hypoxia This represents the amount of oxygen left in the blood after passage through the tissues, and generally indicates the balance between oxygen delivery and consumption Arterial oxygen content is discussed in

☞page 36 Normally, only 20-30% of the oxygen in arterial blood is extracted by the tissues (oxygen extraction ratio,

saturation can be estimated from that in a sample from a

values result if oxygen delivery falls (a fall in arterial oxygen

Hypoxaemic (type I) respiratory failure

Acute hypoxaemic (type I) respiratory failure derives

from one or more of the following four pathophysiological

mechanisms:

The first and most common mechanism is due to

ventilation/perfusion mismatching, which is explained

above This occurs when alveolar units are poorly

ventilated in relation to their perfusion (low Va/Q

units) As the degree of Va/Q maldistribution increases,

hypoxaemia worsens because a greater proportion of the

cardiac output (CO) remains poorly oxygenated

The second mechanism, diffusion impairment, results from

increased thickness of the alveolar capillary membrane,

short capillary transit time (e.g very heavy exercise or

hyperdynamic states, with blood crossing the alveolar

capillaries too fast to pick up much oxygen), and a

reduction in the pulmonary capillary blood volume It very

rarely occurs in clinical practice

The third mechanism is (regional) alveolar hypoventilation,

which ‘fills alveoli with CO2 and leaves less space for

oxygen’ (see above).

The fourth mechanism is true shunt, where deoxygenated

mixed venous blood bypasses ventilated alveoli, results in

‘venous admixture’ Some of this comes from bronchial

blood draining into the pulmonary veins (see above)

This can worsen hypoxaemia – but isn’t really part of

‘respiratory failure’ This is probably all you need to know,

but if you want to know more:

Respiratory failure | 25

24 | Respiratory failure

However, if a patient’s alveolar ventilation is reduced relative

fewer breaths and/or (especially) smaller breaths, when

a greater proportion of each breath is just ventilating the

There are three major causes of (ventilator pump) failure leading to hypercapnia:

1 Central depression of respiratory drive

(e.g brainstem lesions, opiods, Pickwickian syndrome);

2 Uncompensated increases in dead space These

can be anatomical (e.g equipment like endotracheal tube, Heat and Moisture Exchangers (HME)

[☞page 51]) or due to ventilation perfusion mismatch

with high V/Q: here, much of the ventilation is into poorly perfused alveoli which, having limited CO2

delivery to them, act as a dead space;

3 Reduced respiratory muscle strength from neuromuscular diseases (for instance, failed motor

conduction to respiratory muscles as in spinal cord damage, or peripheral neuropathy such as Guillain-Barre Syndrome) or muscle wasting (e.g malnutrition, cancer cachexia, or Intensive Care Acquired Weakness);

4 Respiratory muscle fatigue PI is the mean tidal inspiratory pressure developed by the inspiratory

muscles per breath, while Pmax is the maximum inspiratory pressure possible – an index of ventilator neuromuscular competence The work of breathing increases as overall ventilation (VE) rises, or as PI rises due to increased elastic load (stiff lungs, pulmonary

content or in cardiac output) or if metabolic demands

arterial oxygen content by blood transfusion (to achieve a

fluids and/or inotropes) can thus sometimes help arterial

The Fick equation for VO2 helps to interpret the SvO2:

SvO2 = SaO2 – (VO2/CO)

where CO is cardiac output, (litres/minute) and VO2 is

body oxygen consumption/minute This means that, for

a given arterial saturation, an increase of the ratio VO2/

CO (increase in VO2 or a decrease in CO) will result in a

decrease of SvO2

The relationship between O2ER and SvO2 is apparent

from the following equation:

O2ER = SaO2 – SvO2/SaO2

Therefore, global and regional SvO2 can represent O2ER

Box 1 Relationship between cardiac oxygen consumption, oxygen

extraction and mixed venous saturation

The hypoxia of type I respiratory failure is often associated

respiratory muscle fatigue or CNS impairment ensue, and

minute ventilation falls

Hypercapnic (Type II) respiratory failure

Respiratory failure | 27

26 | Respiratory failure

alveolar ventilation (Va) is:

PaCO2 = kVCO2/VA; PaCO2 = kVCO2/VE-VD

PaCO2 = kVCO2/VT f (1-VD-VT)

where k is a mathematical constant (‘fudge factor’) VE is

minute ventilation and VD dead space ventilation, VT is tidal volume and f respiratory frequency Therefore,

at constant VCO2 and VD , VA depends on VT or f Thismeans that hypercarbia can be caused by four possible conditions:

1 Unchanged total ventilation with decreased f,

2 Unchanged total ventilation with increased f,

3 Decreased total ventilation with decreased f, or

4 Decreased VT

If f increases in the context of unchanged total ventilation

Indices of oxygenation and ventilation

The most common indices you might hear talked about are:

The alveolar to arterial (P (A-a) ) O 2 gradient is the

difference between alveolar PAO2 (calculated using the alveolar gas equation, PAO2 = PIO2 – (PaCO 2 /R)) and PaO2

oedema) or resistive load (e.g airways obstruction such

as asthma) Note that lying flat, with a big abdomen

(fat, ascites, etc.) also hugely increases ventilatory

workload as a results of diaphragm compromise

Ventilatory work also rises if FRC rises This most commonly

results from airway obstruction, when longer is needed to

insufficient, FRC rises with successive breaths (so called

‘dynamic hyperinflation’) and a positive pressure remains at

the end-expiration (intrinsic PEEP, iPEEP) This increases

ventilatory work, as does the fact that tidal breathing occurs

on a flatter portion of the respiratory compliance curve:

inspiratory muscles are forced to work on an inefficient part

of their force/length relationship In addition, the flattened

diaphragm finds it hard to convert tension to pressure

If ventilatory work is too high, the respiratory muscles will

Severe hypercarbia can cause hypoxaemia (the oxygen in the

In the absence of underlying pulmonary disease, hypoxaemia

accompanying hypoventilation is characterised by normal

other three mechanisms are operative are characterised by

widening of the alveolar/arterial gradient resulting in severe

hypoxemia

If f decreases in the context of unchanged total ventilation

| 29

3 Arterial blood gas analysis, oximetry and capnography

Acid-base balance and buffering

The pH of a body fluid reflects hydrogen ion concentration

the action of buffers, including Hb and albumin Phosphate

(weak) acid/bicarbonate buffer pair being of far greater importance:

H+ + HCO3- <-> H2CO3 <-> H2O + CO2

pH will become abnormal (‘metabolic acidosis’) The first response is a rise in minute ventilation (respiratory rate

mandatorily ventilated, then you can do this for them In the longer term (usually days), renal compensation occurs: respiratory acidosis (in COPD, for instance) may thus be compensated for by renal bicarbonate retention

and represents the number of mEq of buffer which would

28 | Respiratory failure

The normal A-a gradient for a patient breathing room air

is approximately 2.5 + (0.21 x age in years), but influenced

by FiO2

The respiratory index, calculated by dividing P(A-a)O2

gradient by PaO2, is less affected by the FiO2 It normally

varies from 0.74-0.77 when FiO2 is 0.21 to 0.80-0.82 when

on FiO2 of 1

The PaO 2 /FiO 2 ratio is easy to calculate, and a good

estimate of shunt fraction A PaO2/FiO2 ratio of

<300 mmHg (40 kPa) is a criterion used to define ARDS,

according to the recent definition (Berlin definition of

ARDS, 2012) (☞page 176) The lower the PaO2/FiO2

ratio, the greater the shunt fraction, meaning that a

greater proportion of the blood that travels though the

lung parenchyma is not in contact with ventilated (and

oxygenated) alveoli For example a PaO2/FiO2 ratio

<300-201 mmHg (40-26.8 kPa) corresponds approximately

to a shunt fraction of 20%, a PaO2/FiO2 ratio 200-101

mmHg (26.6-13.5 kPa) corresponds approximately to a

shunt fraction of 30%, and PaO2/FiO2 ratio <100 mmHg

(<13 kPa) corresponds to a shunt fraction of >40%

Oxygenation index (OI) ) takes mean airway pressure into

account and is calculated as:

OI = (FiO2 x Paw x 100)/PaO2

Dead space ventilation

Dead space is the portion of minute ventilation that does

not participate in gas exchange Its calculation is based on

the difference between end-tidal CO2 (PECO2) and PaCO2,

using the Bohr equation; Vd/Vt = (PaCO2 – PECO2)/PaCO2

In normal conditions Vd/Vt is 0.2 to 0.4

Arterial blood gas analysis, oximetry and capnography | 31

30 | Arterial blood gas analysis, oximetry and capnography

Think of Normal (0.9%) Saline (NS) It contains 154mEq/L of Na+ – only 10% more than the Na+

concentration in your blood (140mEq/L) But the chloride concentration in NS is also 154mEq/L – 54% more than that in your blood (normally perhaps 100mEq/L) Three litres of NS thus raises your [Na+]

a little… and your [Cl-] a lot… bicarbonate levels will fall… and pH will fall

If all these are normal, check the anion gap – the difference

between the concentration of routinely measured anions and

Thus, hyperchloraemic acidosis has a normal anion gap, and lactic – and keto-acidosis (being unmeasured) a raised anion gap If none of these are the cause, then it is possible that some exogenous acid (aspirin, for instance) is in the

Table 1

Increased anion gap Normal anion gap

Ingestion of acid: salicylate poisoning, ethanol and methanol

Loss of bicarbonate via GI tract: diarrhoea/ileostomy

Lactic- or keto-acidosis Renal problems: renal tubular

acidosisInability to excrete acid: renal

failure

Respiratory Acidosis

failure)

restore pH – and the patient’s blood is thus ‘too acid’

Metabolic acidosis

This can result from:

Too little bicarbonate

or loss from small bowel fistulae)

• reduced bicarbonate production (e.g renal failure)

Too much acid

• excess acid production (for instance, lactic acid

production by tumours or from regional or global

ischaemia; ketoacids in diabetic ketoacidosis)

• reduced acid clearance (e.g liver failure), or

• excess acid ingestion (most unusual!)

When faced with a metabolic acidosis, one should thus

establish that:

• The blood sugar levels are and have been normal

(to exclude diabetic ketoacidosis)

• The lactate is normal (to exclude a lactic acidosis)

• Renal function is normal (or, if not, is unlikely to be

the sole cause of the acidosis)

• That the chloride is normal Electrical neutrality must

be maintained in the blood If Cl- rich solutions are

given (such as Normal saline, and many colloids),

Cl- levels will rise To maintain electrical neutrality,

bicarbonate levels will fall, and with it pH

Arterial blood gas analysis, oximetry and capnography | 33

32 | Arterial blood gas analysis, oximetry and capnography

1 Look at the K + , Hb and glucose You now won’t miss

a life-threatening potassium/glucose levels, or profound anaemia

2 Look at the PaO2 and arterial oxygen saturations

to determine how hypoxaemic the patient is Note what the inspired oxygen concentration is! (i.e PaO2

of 12kPa, or 95% arterial oxygen saturations breathing 80% oxygen is NOT good! As a ‘rule of thumb’ the expected PaO2 – in the absence of oxygenation defects – should be about 10 kPa less than the inspired oxygen partial pressure i.e 40% FiO2 should result in PaO2 of 30 kPa)

3 Look at the pH: acidosis (<7.35) or alkalosis (>7.45)?

Metabolic Alkalosis

Metabolic alkalosis is characterised by an increase in

bicarbonate with or without a compensatory increase in

• Excess acid loss (such as in pyloric stenosis)

• Excess ingestion of alkali (rare)

• Renal bicarbonate retention (rare)

• As a consequence of hypokalaemia (causing a

shift in H+)

Respiratory alkalosis

Respiratory alkalosis occurs when an increase in ventilatory

increased ventilation is often in response to pain, anxiety,

hypoxia or fever – or when the patient on mechanical

mandatory ventilation is ‘over-ventilated’

Arterial blood gas (ABG) analysis

An ABG sample may be drawn from an indwelling arterial

catheter, or from an ‘arterial stab’ The commonest site

used is the radial artery, although the brachial, femoral and

dorsalis pedis can also be used An ABG is the quickest way

to accurately determine the true level of hypoxaemia It will

also tell you acid-base status, and help you determine the

chloride and glucose levels) Life-threatening changes in

will sometimes do an ABG when you’re not interested in

Arterial blood gas analysis, oximetry and capnography | 35

34 | Arterial blood gas analysis, oximetry and capnography

apply clinical acumen: if, for instance, normalising the PaCO2 causes a marked alkalosis, and the bicarbonate was high, a metabolically-compensated respiratory acidosis or a respiratory-compensated metabolic alkalosis, were present Your call as to which!

6 Measure the anion gap.

Carbon monoxide poisoning

Carbon monoxide often comes from faulty boilers, smoke inhalation, or suicide attempts from breathing exhaust fumes from cars without catalytic converters

It causes hypoxia because its affinity for Hb is 240 times greater than that of O2

The pulse oximeter, however, doesn’t know the difference between oxyhaemoglobin and carboxyhaemoglobin (COHb) Therefore a grossly hypoxic patient may appear to have ‘normal’ oxygen saturations In addition, the presence of carbon monoxide reduces the amount of O2 released from the blood, as it shifts the O2 dissociation curve to the left

Fortunately most ABG analysers will check for COHb levels – and these are usually <1.5% non-smokers, and

<9% for smokers It is worth remembering that the life of COHb is 5-6 hours, and therefore prompt analysis

half-is indicated if suspected

4 Is the PaCO2 abnormal? If so, has it changed in a

direction which accounts for the altered pH?

5 Is the HCO3- abnormal? If yes, is the change in the

same direction as the pH?

In the ‘not mechanically ventilated’ patient:

• An alkalosis with a low bicarbonate and a low PaCO2

is likely to reflect a primary respiratory alkalosis with

incomplete metabolic compensation

• An acidosis with high bicarbonate and high PaCO2 a

primary respiratory acidosis with incomplete metabolic

compensation

• An alkalosis with high bicarbonate and a high PaCO2

is likely to reflect a primary metabolic alkalosis with

incomplete respiratory compensation

• An acidosis with low bicarbonate and high PCO2 a

primary metabolic acidosis with incomplete respiratory

The problem comes with mechanical ventilatory

support, which alters PaCO2 levels One then has to

Arterial blood gas analysis, oximetry and capnography | 37

36 | Arterial blood gas analysis, oximetry and capnography

Arterial

Fig 2 Oxy-haemoglobin dissociation curve

g/L), and not in solution – is thus:

O2 content = SaO2 x 1.34 x Hb

Unexpected results

ABG analysers use small amounts of blood and perform

a relatively broad range of tests Erroneous results may

be obtained from time-to-time An air-bubble caught

in the syringe may go unnoticed thus raising the PO2,

and similarly Hb or potassium levels may be significantly

deranged from previous readings These uncertainties

are usually best dealt with straight away by repeating

the measurement with a fresh sample – something

easily done with an arterial line in situ If concern

persists, repeat analysis using a different machine

if possible

Arterial oxygen saturation and content

Hypoxaemia can be detected by ABG analysis Alternatively,

pulse oximetry is often used to monitor oxygen saturation

oxy-haemoglobin dissociation curve – the percentage saturation

in the plasma The curve can shift in response to a variety

less willing to release it A ‘right’ shift means that saturation

(☞Fig 2 , opposite).

Arterial blood gas analysis, oximetry and capnography | 39

38 | Arterial blood gas analysis, oximetry and capnography

(air is 21% O2, so FiO2 is 0.21) As a good rule of thumb, PaO2 = FiO2 (%) minus 10 You breathe air, so you’d expect your PaO2 to be about 11 kPa So if someone

is on 60% FiO2 by mask, you’d expect PaO2 to be ~50 kPa If the SaO2 is 94%, then PaO2 is probably only ~9 kPa (when it should be ~50 kPa) Something is terribly wrong with the lungs, and the patient much more seriously ill than they might look!

Capnography

exhaled gas (most commonly by infrared absorption) Two sorts of capnograph exist:

a Sidestream systems (the commonest) continually

aspirate gas from the ventilatory circuit though a capillary tube The CO2 sensor and analyser are located

in the main unit away from the airway

Advantages: it can be used on awake patients, and with

O2 delivery through nasal prongs

b In mainstream systems (much bulkier), the CO2 sensorlies between the breathing circuit and the endotracheal tube

Advantages: no need for gas sampling, and no delay in

recording

O 2 delivery to tissues per minute will thus be oxygen

content per litre x cardiac output (litres/minute) CO can

be ‘indexed’ (CI) to body surface area, and is normally

2.5-3.5 L/min/m2

Oxygen delivery index = DO2I = CI x CaO2

Presuming CI = 3 l/min/m2 and Hb 140g/l,

and SaO2 98%, then

DO2I = 3 x (1.34 x Hb x SaO2 )

DO2I = 3 x (1.34 x 140 x 0.98)

DO2I = 550 ml/min/m2

Top tips on O2 saturation

1 Oxygenation is a very poor measure of ventilation.

Monitoring SaO2 in Guillain-Barre, or severe asthma, or

spinal cord injury thus tells you little about how badly

they are ventilating By the time the SaO2 falls, the

patient is likely to rapidly decompensate

2 Learn a few key points on the O2 dissociation

curve: 99% SaO2 is upwards of 11 kPa Below 8 kPa,

SaO2 starts to fall fast (from about 90%) for a small

change in PaO2 80% SaO2 is approximately 6 kPa

3 Always think of SaO2 in the context of the

inspired fractional O2 concentration, or FiO2

Arterial blood gas analysis, oximetry and capnography | 41

40 | Arterial blood gas analysis, oximetry and capnography

Fig 3 Capnogram

During inspiration, CO 2 is zero and thus inspiration is displayed

at the zero baseline Phase I occurs as exhalation begins B) At the beginning of exhalation, the lack of exhaled CO 2

(A-represent gas in the conducting airways (with no CO 2 ) During Phase II rapid rise (B-C) in CO 2 concentration as anatomical dead space is replaced with alveolar gas, leading to Phase III (C-D) all of the gas passing by the CO 2 sensor is alveolar gas which causes the capnograph to flatten out This is often called the Alveolar Plateau The End Tidal CO 2 is the value at end exhalation Phase 0 is inspiration and marked by a rapid downward direction of the capnograph (D-E) This downward stroke corresponds to the fresh gas which is free of carbon dioxide (except in case of rebreathing) The capnograph will then remain at zero baseline throughout inspiration.

time, the resulting capnogram exhibiting three distinct

phases:

• Phase I occurs at the beginning of expiration when

the anatomic dead space (where no gas exchanges

between inspired gases and blood) empties

• Phase II is the initial rise in CO2 which results from the

mixing of alveolar gas with dead space gas

• Phase III is almost always a slow-rising plateau,

and ends with end-tidal CO 2 (ETCO 2) This is normally

35-38 mmHg (4.5-5 kPa)

After phase III is completed, the capnogram descends

(☞Fig 3 , opposite)

Clinical applications

Capnography reflects the production (metabolism),

thus be altered by changes in:

a Cellular metabolism

Levels may thus rise with increases in temperature

(e.g malignant hyperthermia) or muscle activity (e.g

shivering, convulsions), or increased buffering of acid

(ischaemia-reperfusion, administration of bicarbonate);

b Transportation of CO2

End-tidal CO2 will decrease if CO decreases with

constant ventilation (e.g pulmonary [clot or air]

embolism or sudden cardiac impairment);

c Ventilation

The trace can confirm endotracheal placement, and can be used as a surrogate for ABG analysis Sudden decreases in the ETCO2 may point toward total occlusion or accidental extubation of the endotracheal tube

Capnography is most often used to ensure correct placement

oesophageal intubation) Measurements can also act as

Arterial blood gas analysis, oximetry and capnography | 43

42 | Arterial blood gas analysis, oximetry and capnography

(☞Fig 3 , page 41 )

Causes of raised (PaCO2 – ETCO2) gradient:

• Increased anatomic dead space:

Open ventilatory circuitShallow breathing

• Increased physiological dead space:

Obstructive lung disease

• Low cardiac output states

and there is low inspired volume or high CO But this is really

very uncommon

after each change in ventilator setting, as this can affect the

gradient

In cases of increased intracranial pressure, capnography is

used to adjust ventilation in order to maintain the desired

Supplemental oxygen therapy | 45

44 |

4

Supplemental oxygen therapy

commensurate with survival and, ideally, with unimpaired

organ function This may require intervention to sustain

maintain arterial oxygen saturation The simplest of these is

the administration of supplemental oxygen

Supplemental oxygen therapy

O2 administration is a simple life-saving intervention,

although targeting a PaO2 greater than needed does not

confer additional benefits and high PaO2 can be associated

with worse outcome in certain conditions (e.g., after

cardiac-arrest or myocardial infarction) On the other

hand, one only has to consider the familiar sigmoid shape

of the oxygen dissociation curve (☞page 37) to see that

a failure to administer adequate O2 may have disastrous

consequences – the hypoxaemic patient balances

precariously at the top of the sigmoid precipice, and it

may only take a small reduction in PaO2 to dramatically

decrease SaO2 and tissue O2 delivery (☞page 37)

O2 requirements can be assessed by considering O2

delivery at the bedside: the SaO2, PaO2 on arterial gas

sampling, CO, and Hb This should be balanced against

how much work is going into delivering it (respiratory rate,

work of breathing), and whether it is sufficient (rising lactate suggests anaerobic metabolism: confusion and oliguria may suggest hypoxic organ dysfunction)

The target of O2 therapy should be to give enough O2 to return the PaO2 to the level required by that particular patient In practice, this usually means aiming for SaO2

94-98% In general, however, high flow O 2 is indicated

in shock, sepsis, major trauma, anaphylaxis, major pulmonary haemorrhage and carbon monoxide poisoning

NB hyperoxia may worsen outcome after cardiac arrest and should be avoided In patients with chronic hypercapnia,

lower FiO 2 may be needed with target SaO 2 of 88-92%

In these patients, the effects of high FiO2 in determining hypercapnia are multiple:

1 Reduction in hypoxic ventilatory drive (some with COPD, cystic fibrosis, neuromuscular / chest wall disorders, obesity hypoventilation syndrome / morbid obesity: ☞page 25)

2 Reduction in hypoxic pulmonary vasoconstriction and increase in dead space ventilation

3 Haldane effect: this is the displacement of CO2

bound to the deoxygenated Hb, which is released in the plasma and accumulates as a result of chronic hypoxaemia

A look at the initial ABG may be helpful in guiding you:

if PaCO2 is raised, but pH less deranged than you might expect (with a high blood bicarbonate), then chronic

hypoventilation is likely (☞page 24) Here, and if you are

confident that hypoxaemia isn’t life-threatening, FiO2 28%

Supplemental oxygen therapy | 47

46 | Supplemental oxygen therapy

may be initiated, seeking SaO2 targets of 88-92% Regular

monitoring of ABGs is essential in this group of patients,

because persistent acidosis and hypercapnia may require

non-invasive ventilatory support or possibly intubation

Whilst students are often warned about the patient

dependent upon hypoxic ventilatory drive (☞page 25)

who dies when supplemental O2 is given, this is a rarity:

in the severely hypoxaemic patient, one should err on

the side of giving higher concentrations of O2 if hypoxia

seems grave, and then reducing it according to clinical

response and ABG analysis If there is only a mild degree

of hypoxaemia (or if the hypoxaemia seems oddly well

tolerated, suggesting that it may well be chronic), it

may be more suitable to deliver low dose O2 via nasal

cannulae Note: if a patient is cerebrating well, then

the gases you see are likely ‘closer to their normal’ and

needn’t precipitate panicked responses!

Non-invasive O2 supplementation can be provided via

nasal cannulae or face masks A variety of O2-delivery

devices exist, and it is helpful to know their relative pros

and cons However, the FiO2 actually inhaled depends

not only on the magnitude of flow of O2 into the airway

but on the respiratory rate, tidal volume and hence

minute ventilation, i.e giving 2 L/min to a normal patient

breathing at rest (RR =12/min x TV = 500ml = Minute

Ventilation 6 L/min) will increase their inspired oxygen

fraction far more than will the same 2 L/min given to a

tachypnoeic patient (e.g RR 36) This is not just a simple

issue of ‘concentration’ High respiratory rates often mean

high inspiratory flow rates (i.e gas moves fast on breathing in) Let’s suppose that the peak inspiratory flow rate is 60 L/min If O2 is being delivered at 15 L/min (without some reservoir), then ordinary room air will be entrained during inspiration The TRUE FiO2 will thus be a lot lower than you imagined!

• Variable performance systems

(Nasal cannulae, Hudson face masks)

• Fixed performance systems

(Venturi-type masks)

• High Flow systems

• Others

Nasal cannulae (like simple face masks) use the dead

space of the naso-pharynx (or the device themselves)

as an O2 reservoir Entrained air mixes with the air in the reservoir and the inspired gas is enriched with O2 For most patients, and as a general rule of thumb, each additional 1 L/min of O2 flow via nasal cannulae increases FiO2 by ~ 4% The maximum amount of O2

that can be administered via nasal cannulae is 6 L/min i.e approximately 45% O2 Advantages include comfort and easy retention (not removed to speak, eat or drink) However, it is hard to accurately gauge FiO2 Nasal congestion impairs use, and nasal drying and irritation can occur

Simple face masks (e.g Hudson masks) deliver O2

concentrations between 40% and 60% The FiO2 supplied will be inconsistent, depending on the flow rate and the

Supplemental oxygen therapy | 49

48 | Supplemental oxygen therapy

Venturi masks provided an estimate of FiO2 regardless

of the flow rate (as long as it is above the minimum stated on the side of the valve) – although the EFFECTIVE FiO2 may still be influenced by the patient’s respiratory rate and pattern, particularly at higher FiO2 Slits found

on the side of an attachment allow air to be entrained

(☞Fig 5, below) Their size (and degree of entrainment)

varies, as does the diameter of the O2 entry point The amount of entrained air is directly affected by the flow

of O2 into it, with different masks permitting selected flow rates of O2 in spite of different amounts of gas being drawn in There are a variety of colour – coded valves – 24% (Blue), 28% (White), 35% (Yellow), 40%

(Red), 60% (Green) – and they are particularly useful when there is a need to control the amount of O2 being

delivered e.g in COPD (☞Fig 6, page 50)

Air

Air

Fig 5 The Venturi Principle

patient’s breathing pattern (see above), but can be changed

using O2 flow rates of 5-10 L/min Flow rates less than 5

L/min can cause exhaled CO2 to build up within the mask

(which is thus a sort of dead space, ☞page 25) and thus

to rebreathing For these reasons, and the consideration

made previously, such masks are often avoided in those

with Type 2 respiratory failure

High concentration reservoir masks deliver O2 at

concentrations of 60-90% and are used with a flow rate

of 10-15 L/min A bag acts as a reservoir of 100% O2

from which to draw (thus overcoming the ‘entrainment’

problem outlined above) However, once again, the inspired

concentration is not accurately measured and will depend

on the pattern of breathing These masks are used in the

emergency or trauma patient where high flow O2 is required

and where CO2 retention is unlikely (☞Fig 4, below)

Fig 4 High concentration reservoir mask (non-rebreathing)

When a patient breathes through the nose, the inspired air

is warmed to body temperature and becomes saturated with water vapour before entering the trachea Medical gases have very low moisture content and, delivered via endotracheal tube or tracheostomy, cool and dry the lower airway Mucus becomes thicker (‘plugging’ airways) The airway epithelium becomes desiccated, causing ciliary mucus transport to fail, and thence epithelial denudation The risk of atelectasis, lobar collapse and infection then rises

To avoid such consequences, inspired gases must be warmed and humidified Active devices, such as heated humidifiers, add warm water vapour to a flow of gas independent of the patient Passive devices, such as heat and moisture exchangers (HME), retain some of the heat and moisture which would otherwise be expired, to warm incoming gas Standards for humidifiers used with intubated patients specify that they must have a moisture output of at least

equivalent to that measured in the subglottic space during normal nasal breathing Few HMEs have a moisture output

at this level However, HMEs are cheaper and easier to use

Passive devices

Heat and moisture exchangers are most commonly used,

and each is a disposable ‘single patient’ device Some designs can also filter out bacteria, viruses and particles in

Fig 6 Venturi mask with various valves

Humidification | 53

52 | Humidification

Active devices

The simplest method of humidifying the inspired gases is

through the instillation of water directly into the trachea

ETT each hour, or by ‘drip-instilling’ a set volume each hour This is sometimes done when secretions are very thick and can help greatly in removing the rubbery bronchial casts of asthma

Heated humidifiers (e.g Fisher-Paykel systems) have two

separate electrically-powered active heating systems

Firstly, a water chamber sits on a heater plate Gas passes through this chamber, and then over a heater wire in the centre of the hose leading to the patient Two sensor monitors gas temperature at the patient connection port and humidification chamber outlet respectively, and control heater wire temperature

The temperature of the gas required at the patient-end

of the delivery tube can thus be varied, as can relative humidity: if the temperature of the gas to be delivered to the patient connection port is to set to be higher that at the humidifier end of the delivery tube, the gas is warmed

as it passes through the delivery tube Condensation is therefore reduced, but the relative humidity of the gas also decreases Alternatively, if the gas is allowed to cool as it passes through the delivery tube, it will be fully saturated with water vapour

A water trap collects condensation in the expiratory limb The humidifier and the water trap should be positioned below the level of the tracheal tube to prevent flooding of the airway by condensed water

either direction of gas flow, being called Heat and Moisture

Exchanging Filters (HMEF) Positioned at the ventilator

circuit ‘Y connector’, one port connects to the inspiratory

limb and the other to the ‘ETT’ side of the ventilator circuit

Inside this unit is material impregnated with a hygroscopic

substance When warm moist expired gases pass through

this element, water condenses – the latent heat release of

which also warms it During inspiration, cool dry air passes

through the element – and is warmed and humidified – the

element thus acting as an ‘artificial nose’ Optimal function is

HMEs may be best avoided when:

• Tidal volumes are small (when the HME’s additional

dead space can lead to increases in PaCO2)

• Secretions are thick, copious, or bloody, when they

may be deposited on the moisture exchanging

element, increasing the resistance to breathing,

affecting the ability to wean from the ventilator and

perhaps altering ‘trigger sensitivity’ (☞chapter 12)

Secretion deposition can also increase the risk of

infection with organisms such as pseudomonas

• When ventilatory volumes are very high (when they

become inefficient)

• When core body temperature is <32°C (when they

fail to work effectively)

• When expired volume is <70 % of delivered tidal

volume (bronchopleural fistula)

Back to contents Back to contents

54 | Humidification

Back to contents

| 55

6 Assessing the need for ventilatory support

There are three main indications for mechanical ventilation:

1 To support oxygenation (by improving deliveryand/or reducing consumption through work of breathing)

2 To support CO2 clearance, and

3 Reduce the work of breathing – assisting or ‘resting’ the respiratory muscles

In addition, mechanical ventilation is sometimes needed as part of a package of care in managing the patient who is combative or restless (e.g the agitated combative patient with multiple trauma)

Assisting with oxygenation

Cardiac output (in litres/min) x SaO2 x 1.34 x Hb

(☞page 38 ) You can usually determine Hb and SaO2 easily enough, and can estimate cardiac output from the heart rate

The heated element humidifier drips water onto an electric

element heated to 100°C, the high temperature ensuring

sterility A water trap collects excess water The amount of

the water vapour delivered from these humidifiers must be

controlled according to the minute volume and humidity

required

Nebulisers may be gas-driven or ultrasonic (☞page 148)

In both devices, droplets are produced; ideally with a

diameter of about 1 µm Droplets evaporate in the gas

delivered to the patient so that the gas is fully saturated

with the water vapour As heat is required for the

evaporation, the temperature of the gas falls A heater can

maintain the desired temperature of the gas However,

with these devices, it is relatively easy to add excessive

moisture to the delivered gas, as some of the droplets do

not evaporate, leading to the risk of excessive loading of

the lungs with water

Assessing the need for ventilatory support | 57

56 | Assessing the need for ventilatory support

Increasing Delivery can be achieved by the use of

supplemental oxygenation, other techniques to improve

oxygenation (e.g., the use of PEEP (☞page 54), recruitment manoeuvres (☞page 133), or altered I:E

ratios, raising Hb concentration, and increasing the CO (with the use of fluids and/or inotropes where indicated)

Mechanical ventilation can help address both sides of the equation Muscle activity in the sedated patient is lower, and reduced further if the patient is pharmacologically paralysed Work of breathing – a potent consumer of oxygen – is also limited Thus, at rest, about 4ml in every 100ml of oxygen your body is using is consumed by the work of breathing In a patient after thoracic surgery, this might double, whilst in severe COPD or pulmonary oedema, work increases even more

Sometimes, work of breathing exceeds capacity, and minute

In such circumstances, the addition of ventilator support can aid in maximising alveolar minute ventilation Remember,

emergency support, if the pH is near-normal due to chronic

asthma should be able to maintain minute ventilation – and

might prove rapidly fatal

and a feel for the pulse volume (high, normal or low) That

allows for a rough-and-ready bedside guesstimate of oxygen

delivery

the presence of muscle activity (shivering, restlessness, fits),

fever, and work of breathing (nasal flaring, paradoxical chest

wall movement, big swing on the CVP trace) – all associated

the presence of anaerobic metabolism) or a low oxygen

☞pages 22-23) – but not from a femoral central catheter

delivery relative to demand However, it needs to be kept in

deficiency in certain clinical conditions such as sepsis when

blood

When an imbalance of

O2 demand and O2 delivery exists, one can

address BOTH sides of the equation:

Reducing Demand can be achieved by cooling the

febrile patient (physically or with paracetamol), reducing

work of breathing with nebulisers (if asthmatic), or

offering adequate sedation, neuromuscular paralysis or

analgesia

Back to contents

58 | Assessing the need for ventilatory support

| 59

7 Continuous positive airway pressure (CPAP)

CPAP consists in the application of constant positive airway pressure throughout the respiratory cycle in spontaneously breathing patients Alveoli are like party balloons: when small, they need a lot of work to blow them up, and (especially when small) have a tendency to collapse down and empty Were this to happen, alveoli would collapse at the end of every breath, needing a lot of work to re-expand them with each breath in In addition, some alveoli wouldn’t reinflate with smaller breaths, leading to V:Q mismatch, and hypoxaemia

(☞pages 16, 22 )

Two processes help overcome these problems:

1 Alveoli produce surfactant – a detergent which

lowers the surface tension of the wall This effect increases as alveolar size falls However, lung inflammation damages alveoli, causes proteinaceous fluid to leak into them, and preventing them making surfactant

2 Partial closure of the glottis (and possibly vocal cord

apposition) at the end of expiration ‘traps’ some air

in the lungs, and keeps the pressure in the airways about 3-5 cm H2O greater than atmospheric pressure This positive pressure within the alveoli at the end

of expiration is known as ‘Positive End-Expiratory Pressure’ or PEEP, and helps hold them open

Assisting with the agitated patient

Sometimes, mechanical ventilation is instigated when ‘the

lungs are fine’ Thus, an agitated patient who won’t lie still

for a CT head scan may need to be paralysed, intubated

and ventilated The same holds true, for instance, of the

bomb victim with severe injuries, who is trying to launch

themselves to the floor – preventing central line insertion

and appropriate assessment and management

Continuous positive airway pressure (CPAP) | 61

60 | Continuous positive airway pressure (CPAP)

time the mouth is open In most patients with acute respiratory failure, full face masks are a more appropriate choice Masks are usually made from non-irritant material such as silicon rubber, and have minimal dead space and soft (usually inflatable) cuffs to provide a seal with the skin All masks exert pressure on the nasal bridge, and can cause ulceration A ‘full head helmet’ system overcomes this problem

2 A continuous flow of gas at a flow rate which exceeds peak inspiratory flow rate at all times Otherwise, the

pressure in the system will fall on inspiration

3 A system for humidifying the delivered gas, if used for

prolonged periods

4 A valve at the outlet of the system, which maintains a pre-determined pressure (often 5, 7.5 or 10 cmH2O) However CPAP can be provided using a variety of standard ICU ventilators using the non-invasive

modality (☞Fig 7, below)

Patient’s Face

Tight-fitting maskFlow Generator

Flow at rate > patient’s peak inspiratory flow rate

Valve to regulate pressure(= flow x resistance)

Fig 7 Diagram of CPAP circuit

Endotracheal intubation holds the glottis and cords

open, so PEEP is lost and alveoli tend to collapse unless

we apply this PEEP artificially (☞page 59)

When alveoli collapse, local ventilation falls while local

perfusion may be sustained – the resulting V:Q mismatch

overcome by augmenting airway pressure with a continuous

‘extra pressure’ throughout the respiratory cycle Continuous

positive airway pressure (CPAP) increases FRC, reduces V:Q

mismatch, and improves oxygenation Work of breathing may

be reduced by maintaining a mouth-to-alveolar gradient,

and by helping keep alveoli open In addition CPAP has

cardiovascular effects reducing cardiac preload and reduce

the left ventricular afterload by decreasing the left ventricular

transmural pressure These effects are advantageous in

patients with cardiogenic pulmonary oedema

Measures of ‘success’ in using CPAP are thus:

a Improvement in respiratory pattern (due to

improved oxygenation and reduced work of breathing

relieving dyspnoea)

b Improvement in oxygenation

To work, CPAP needs:

1 A sealed system Thus, masks are tight-fitting and

leak-free

Facemasks and nasal masks are both used Patients

often prefer nasal masks, but must keep their mouths

closed, as positive airway pressure is lost every

Continuous positive airway pressure (CPAP) | 63

62 | Continuous positive airway pressure (CPAP)

hair can be a problem – perhaps resolved by shaving them (with consent)

When applying the face mask, it may be helpful to first allow the patient to hold it on themselves, as many patients may feel claustrophobic The mask is then held on the face

by the harness which passes around the back of the head When tightening the straps, it is important to find a balance between leaving the mask loose and having a large leak and

usually slightly higher than that the patient received prior to

Not every hypoxaemic patient benefits from CPAP In simple asthma, for instance, hypoxaemia is due to the plugging of small airways with thick sputum CPAP will generally not resolve these issues, hinders humidification and use of nebulisers, and may also worsen overexpansion of other lung units ‘Solid or blocked lung’ (e.g lobar consolidation due to tumour or pneumonia) may have little gain, as the alveoli cannot be ‘reopened’ In such circumstances, application of CPAP may cause distress and be of limited advantage Some COPD patients may benefit – but others may suffer hyperinflation of lung units, and thus a worsening of ventilation However, this is often very hard

to predict –and a trial of treatment is usually warranted:

require intubation if they are tried on CPAP or NIV

(☞chapters 7 and 8 )

CPAP may improve oxygenation and its primary role is thus

in Type I (hypoxaemic) respiratory failure However, CPAP may also splint the upper airway open in patients with obstructive sleep apnoea, thus preventing the occurrence of

Fig 8a Face mask

Fig 8b CPAP valve and harness

Some patients are not suited to the use of CPAP masks,

perhaps due to agitation or shape of face (a receding or

prominent lower jaw may prove difficult) Extensive facial

Non-invasive ventilatory support (NIV) | 65

64 | Continuous positive airway pressure (CPAP)

8 Non-invasive ventilation (NIV)

‘ventilatory’ support, colloquially, people usually mean ‘some form of positive pressure support’ when talking about non-invasive ventilation, or ‘NIV’ This ‘pressure support’ is needed when the work of breathing exceeds the patient’s capacity to perform – due to weak or impaired muscle contraction (e.g Guillain-Barre), very high work of breathing (e.g massive ascites compressing the diaphragm, pulmonary oedema), or a combination (e.g the cachectic COPD patient)

Normally, contraction of the inspiratory muscles expands the thoracic cavity volume, reducing intra-pleural, interstitial, and alveolar pressures further below atmospheric Air is thus drawn into the lungs from the mouth cavity (which is,

of course, at atmospheric pressure) Appropriate equipment can sense the start of gas flow (‘flow sensing’) or, more generally, the fall in pressure (‘pressure sensing’), recognise

it as the start of inspiration, and apply positive pressure

at the mouth The pressure gradient between mouth and alveoli is thus increased, gas flow into the lung augmented (with preferential inflation of the most compliant areas of the lung), and the inspiratory work of breathing reduced Generally, this inspiratory positive pressure is used together with an elevated expiratory pressure (PEEP), helping to hold alveoli open When applied by mask, this combination

of PEEP and pressure support is often referred to as Invasive Ventilation’ or ‘NIV’ for short

‘Non-nocturnal desaturation and hypercarbia In other conditions,

too, alveolar recruitment may increase tidal and minute

may diminish alveolar ventilation, and respiratory muscle

ventilation are needed

Complications of CPAP

CPAP is generally safe Infrequent complications include

pressure necrosis of skin, especially of the nasal bridge

Early application of a colloid dressing (or similar) may

help avoid this Under pressure, air can be swallowed,

and gastric distension is not uncommon This may

cause discomfort, while resulting splinting of the

diaphragm can cause basal atelectasis If CPAP use

is to be prolonged, parallel use of a nasogastric tube

may be considered – although this may in fact worsen

gastric distension by ‘opening a track’ through the

cardiac sphincter Air leak upwards may lead to corneal/

conjunctival irritation At its worst, ulceration results

This is potentially serious – so care must be taken to

avoid substantial ‘upward leak’ Pneumothorax can

rarely complicate in patients at risk (e.g trauma, COPD)

Non-invasive ventilatory support (NIV) | 67

66 | Non-invasive ventilatory support (NIV)

distal breathing circuit through a side port With this latter

on flow within the circuit, and it is not possible to provide

when treating hypoxaemic patients

Some machines are also capable of trying to deliver a

set volume of air with each breath (up to a set maximum

pressure) – by controlling inspiratory flow rate of gases, and duration of the inspiratory cycle (i.e gas continues to

be pushed in at a set rate and time, to deliver a set volume) – but such machines aren not able to recognise leaks around the mask In general, pre-set pressure support and PEEP (as BiPAP) is used

Indications for NIV

By using a completely sealed system in which air cannot

be entrained, CPAP/BiPAP circuits are able to deliver a

effective at treating hypoxia Alveolar recruitment (and fall

indicated when alveolar recruitment may occur, and BiPAP/NIV when work of breathing requires augmentation

The role of both CPAP and NIV in the management of

pulmonary oedema is clearly established A possible

role in asthma is more contentious – and may limit

administration of nebulisers

NIV is often used when the need for ‘ventilatory’

support is likely to be short-lived (acute pulmonary

oedema), or where intubation may carry greater risks

than benefits, or in patients with conditions leading to

chronic type 2 respiratory failure Application of NIV

may prevent the need for endotracheal intubation in

the latter which tends to increase dead space, generally

requires sedation, limits mobility, may be distressing,

and which prevents easy speech, oral nutrition,

self-regulation of fluid intake and other aspects of

self-caring However, NIV should not delay intubation

and mechanical ventilation when this is necessary

Equipment

The basic requirements are a pressure and flow generator

(‘ventilator’), ventilator tubing and the interface to connect

the system to the patient Portable non-invasive ventilators

are widely used, both on the ICU and respiratory wards

Different models of varying complexity are available, although

all are capable of providing high gas flows to maintain preset

airway pressures at the end of expiration (expiratory positive

airway pressure, or EPAP – really just another way of saying

‘PEEP’), as well as sensing the respiratory effort made by the

patient and delivering ‘inspiratory positive airway pressure’

(or IPAP) This application of two pressures is sometimes

referred to as ‘Bilevel Positive Airway Pressure’ – or BiPAP

In most patients with acute respiratory failure, full face

masks are used, and are more effective than nasal masks in

Non-invasive ventilatory support (NIV) | 69

68 | Non-invasive ventilatory support (NIV)

• In chest trauma, NIV may reduce pain by offering some respiratory support

• NIV may also have a role in assisting in early extubation of patients with background of COPD In unselected patients, the use of NIV as a rescue therapy post extubation failure has shown to increase mortality

• Respiratory failure in immunosuppressed patients can have a poor outcome: mortality rates (for instance,

in bone marrow transplant patients) can be >90%

Especially in those with single organ failure due to opportunistic infection, a trial of NIV may improve their outcome by avoiding the risk of superadded ventilator-associated pneumonia Several uncontrolled trials have shown NIV to be successful in about two-thirds of patients with AIDS, haematological malignancies, or pneumonia following lung transplantation

• There is a risk of apnoea

• Head or facial injuries

• Relative contraindications include factors that make it difficult to create a seal with the mask (facial deformity

or recent surgery), conditions where air swallowing may

• In the management of exacerbation of chronic

obstructive pulmonary disease (COPD), NIV is now

the recommended first line therapy for patients with

type 2 respiratory failure Here, acute respiratory failure

is often driven by increased work of breathing from

dynamic airway collapse These factors may prevent

complete exhalation before the next inspiration starts,

and ‘dynamic hyperinflation’ of the lungs results The

result is a positive pressure in the alveoli at the end

of expiration (‘intrinsic PEEP’ climbs) This pressure

needs to be overcome before inspiratory flow can

occur Inspiratory load is thus increased Rapid, shallow

respiration often results, which increases VD/VT

(☞page 28) and this, with respiratory muscle fatigue

causes PaCO2 to rise NIV raises upper airway pressure

reducing airway collapse, dynamic hyperinflation

and intrinsic PEEP Tidal volumes and CO2 clearance

increase, and respiratory rate falls Intubation rates,

mortality and ICU and hospital length of stay are

reduced Those who respond best are symptomatic

patients with moderate respiratory acidosis

(pH 7.25-7.35) in whom treatment is started early

• Use of CPAP in cardiogenic pulmonary oedema recruits

alveoli, reduces V:Q mismatch, improves oxygenation,

and leads to more rapid resolution of symptoms It also

reduces work of breathing, increased by upper airway

oedema, and repeated reopening of collapsed alveoli

Indeed, as much as 70% of total body O2 consumption

may be used by the respiratory muscles alone

BiPAP may be considered, especially if hypercarbia is

indentified, or when work of breathing seems especially

raised

Non-invasive ventilatory support (NIV) | 71

70 | Non-invasive ventilatory support (NIV)

recruitment, facilitate triggering in patients with high intrinsic PEEP

be increased, and should improve tidal volume

It is important to observe the patient while on NIV, to ensure adequate synchronisation with the ventilator Each patient effort should determine an increase in airway pressure and that the inspiratory phase does not continue after the patient starts to exhale The most common cause of asynchrony is mask leaks: appropriate mask fitting is therefore essential

All acute use of NIV should be considered a trial If work

of breathing increases, arterial gases do not improve adequately or worsen, or if there is a deterioration in the level of consciousness or tolerability, tracheal intubation and mechanical ventilation should be considered This is best done ‘electively’, and not when crisis point has been reached

Complications of NIV

Cardiovascular effects of positive pressure ventilation

Normal inspiration is associated with a negative intrathoracic pressure, which draws venous blood into the right atrium, and expands the pulmonary vascular bed, lowering pulmonary vascular resistance and increasing the volume of ‘blood held’

in the lungs Right ventricular stroke volume thus rises a little during slow inspiration, while left ventricular output

cause problems (recent oesophageal/gastric surgery)

and cases where frequent interruption of ventilation is

required in order to clear copious secretions, small or

large bowel obstruction

• There is clear consolidation on the Chest X-ray (NIV

increases mortality)

Practical NIV issues

positive airway pressure) is the total inspiratory pressure

depending of tolerability and degree of mask leaks Most

machines can generate high pressures (although rarely used)

around the mask is usually a problem, and conventional

invasive ventilation may be indicated

As for CPAP, measures of success include:

respiratory rate falls

(due to improved oxygenation and reduced work of

breathing relieving dyspnoea)

and EPAP adjusted to try to improve alveolar

Non-invasive ventilatory support (NIV) | 73

72 | Non-invasive ventilatory support (NIV)

predominate, and how sensitive the heart is to these changes (by nature of cardiac disease, or existing loading/filling conditions) When intravascular volume is normal and intrathoracic pressures are not excessive, the effect on afterload reduction predominates, and positive pressure ventilation increases cardiac stroke output However, in hypovolaemia the predominant effect is to reduce ventricular preload, and CO

Positive pressure ventilation also impedes lymphatic flow: raised pulmonary interstitial pressures (including that from PEEP) compress thin-walled peripheral lymphatics Positive pressure ventilation (and PEEP) can, at high levels, thus increase lung water: PEEP helps remove fluid from alveoli, but the reduction in thoracic duct drainage can result in interstitial fluid retention and pleural effusions Whole body salt and water retention can also be encouraged: high venous pressures encourage oedema, and effects on atrial loading can promote antidiurectic hormone secretion and inhibit release of natiuretic peptides

Such effects are rarely of clinical importance in using NIV, however, and may have greater impacts during prolonged invasive mechanical positive pressure ventilation, with which we shall deal in the following chapters

falls slightly The reverse is true of the expiratory phase

During mandatory positive pressure ventilation there is

an increase in intrathoracic pressure and a fall in venous

return, right ventricular output, and pulmonary blood flow

on inspiration On expiration, the intrathoracic pressure

falls and the venous return increases In other words, the

normal respiratory cycle of cardiac filling and emptying is

reversed Positive intrathoracic pressures from PEEP also

inhibit venous return

Overall, then, positive pressure ventilation means that right

ventricular preload is reduced:

• positive intrathoracic pressure decreases the pressure

gradient for venous inflow into the thorax

• positive pressure exerted on the outer surface of the

heart reduces cardiac distensibility, and this diastolic

ventricular filling

• compression of pulmonary blood vessels raises

pulmonary vascular resistance which impedes right

ventricular (RV) stroke output (i.e increase RV

afterload), causing the RV to dilate, the interventricular

septum to bulge into the left ventricular (LV) cavity,

LV chamber size to fall, and thus LV diastolic filling

to reduce

As a counterbalance, cardiac compressive effects during

systole tend to have a positive effect on systolic ejection,

(‘like the hand squeezing the ventricle during systole’)

Thus, positive-pressure ventilation tends to reduce

ventricular filling during diastole but enhances ventricular

emptying during systole The overall effect on cardiac output

will depend on whether the effect on preload or afterload

Back to contents Back to contents

Artificial airways | 75

74 |

9

Artificial airways

Mandatory mechanical ventilation is hard to deliver

non-invasively A secure airway is thus required This may be

either an orotracheal airway – colloquially known as an

endotracheal tube (naso-tracheal tubes are infrequently

used nowadays), or a tracheostomy

Endotracheal tubes

Endotracheal tubes provide a means of securing a patient’s

airway (i.e ensuring access to the trachea for ventilation,

whilst limiting contamination from the pharynx)

Connector

Balloon (pumps up cuff)

CuffBevel

Fig 9 Endotracheal tube

They are equipped with an inflatable balloon at the distal end

(the cuff) that is used to seal the trachea and prevent positive

pressure inflation volumes from escaping through the larynx, and guard the lungs from the entry of oropharyngeal

or stomach contents from above Whilst the proximal end

to most women The length is marked in centimetres on the

Delayed complications are caused by pressure-induced injury of the surrounding tissues: obstruction of the maxillary antrum causing sinusitis (for nasal intubations), laryngeal or tracheal granulation tissue and obstruction, and tracheal erosion (causing haemorrhage)

Correct position

For orotracheal intubations, the length from the tip to the teeth is normally about 20-22 cm in women and 21-24 cm in men However, a CXR soon after intubation

is mandatory, as entry into the right main bronchus can readily occur, and it is important to assess the height of the tube above the carina A tube ending 3-5 cm above the carina with the head in a neutral position is usually ideal The tube can be ‘cut’ to ensure that it is not too long – although different ICUs sometimes have strong views as to whether to do this or not! Tube length at the lips should be noted, and regular nursing checks made

to ensure that the tube does not slip too far inwards

N.B flexion and extension of the neck causes a 2 cm displacement of the endotracheal tube tip

Artificial airways | 77

76 | Artificial airways

Endotracheal tubes and work of breathing

Resistance to flow through the ETT is directly related to

patients admitted to the ICU A patient who is ventilated

for a more prolonged period may build up biofilm on the

internal lumen and this effectively reduces the working

diameter It should also be remembered that if an ICU

patient needs a bronchoscopy, then it is tricky to safely

a patient is intubated, work of spontaneous breathing is

typically increased It is often stated that pressure support

work of breathing in a non-intubated patient

Endotracheal tubes and ventilator-associated

pneumonia (VAP)

It is becoming increasingly apparent that aspiration of

contaminated oropharyngeal secretions and the development

of a biofilm within the ETT lead to VAP Therefore a variety

of ‘modified’ ETTs are now available, and have been shown

to reduce the incidence of VAP Hence there are two main

strategies used to try to decrease VAP:

1 Reduction of pulmonary aspiration of

oropharyngeal secretions:

a Subglottic secretion drainage:

ETTs with an additional suction port situated

above the cuff to allow aspiration of oropharyngeal

secretions that pool above the cuff;

b Modified (thin) polyurethane-cuffs:

These cuffs limit the formation of folds within the cuff which contribute to microaspiration;

c Cuff pressure measurement:

Numerous devices are now available to maintain cuff pressure within the ideal range of 20-30 cmH2O

2 Reduction in the formation of biofilm on the internal lumen

This is NOT the same as tracheostomy It is a quite different

procedure, in which the trachea is entered through the

cricothyroid membrane

Minitrachs: Access with a small tube (a ‘minitrach’) can aid

suctioning of secretions in those with poor clearance

Needle cricothyroidotomy: This is a life-saving airway

procedure which is undertaken in a time-critical situation

obstructed airway

Briefly, this is how it is done:

• Prepare O2 tubing – either a side hole is cut in the

tubing near one end, or a Y-connector is attached The

other end is connected to an O2 source

• Position the patient supine, with the neck neutral or

slightly extended, and prepare the skin with antiseptic,

and then infiltrate with local anaesthetic (e.g 2ml 1%

lidocaine with adrenaline 1:200,000)

• Attach a 12 (or 14G) IV cannula to a 10ml syringe

• Between the thyroid cartilage and cricoid cartilage,

palpate the cricothyroid membrane in the midline With

the thumb and forefinger of your non-dominant hand

stabilise the trachea to prevent lateral movement

• Puncture the membrane with the needle, directed 45° angle towards the chest, whilst gently aspirating the syringe Aspiration of air confirms entry into the trachea

• Remove the needle whilst carefully advancing the cannula sheath downwards Care must be taken not to perforate the posterior wall of the trachea

• Attach O2 tubing to the hub of the catheter, and secure the catheter to the patient’s neck A vigilant assistant should hold the cannula to prevent kinking Intermittent ventilation is achieved by occlusion of the hole in the tubing for 1 second, then releasing it for 4 seconds

Passive exhalation (via the oro/nasopharynx, not via the cannula) can occur when the hole is not occluded

minutes (the principal limitation being a steady accumulation

assistance or equipment (e.g fibreoptic intubation) is prepared Close observation is mandatory!

Complications include:

• Inadequate ventilation leading to hypoxia and death If the airway is obstructed proximal to the cannula, the patient is unlikely to be able to overcome the obstruction at exhalation and a surgical cricothyroidotomy should be considered immediately

In this situation, only small volumes of O2 should be